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Biomedical subjects

R Kikawada

Publications and source records attributed to R Kikawada.

At least 37 records · Page 2Linked to original sources
PubMed1991

Changes of common fragile sites on chromosomes according to the menstrual cycle.

The frequencies of chromosomal breaks and sister chromatid exchanges (SCE) are influenced by pregnancy, oral hormonal contraceptives and the menstrual cycle. The changes in the number and sites of spontaneous and aphidicolin-induced breaks on chromosomes from peripheral blood lymphocytes during the menstrual cycle were examined in 8 healthy women. Menstrual cycle was determined by menstruation and the quantity of serum estrogen, progesterone and luteinizing hormone. The number of spontaneous breaks at the follicular phase, the interval phase (which includes ovulation) and the luteal phase were 3.1 +/- 1.1, 2.7 +/- 2.3 and 3.9 +/- 2.6 per 100 mitoses, respectively. The frequencies of aphidicolin-induced breaks in the same phases were 95.8 +/- 23.3, 90.6 +/- 14.3 and 122.7 +/- 20.1 per 100 mitoses, respectively. The higher frequency at the luteal phase was statistically significant compared with the other phases. In the luteal phase, bands 2q32, 3q27, 6q26 and 16q23 had higher frequencies of breaks (P less than 0.05); however, breaks at band 9q32 decreased significantly. SCE showed considerable variation, but with no statistical significance.

Adult↗
PubMed1991

The 'oral 1,25-dihydroxyvitamin D3 pulse therapy' in hemodialysis patients with severe secondary hyperparathyroidism.

Many hemodialysis patients are still suffering from secondary hyperparathyroidism although 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) has been used to treat renal osteodystrophy for the last two decades. The main reason for its failure to correct the secondary hyperparathyroidism is that in patients, hypercalcemia occurs before adequate parathyroid hormone (PTH) suppression is obtained when a large daily dose of 1,25(OH)2D3 is started. In this study, the oral dose of 1,25(OH)2D3 (4.0 micrograms) was administered only twice a week at the end of hemodialysis ('oral 1,25(OH)2D3 pulse therapy'), in 19 patients with severe secondary hyperparathyroidism. Serum immunoreactive PTH started to decrease after 6 weeks of therapy, and the original level of 41.2 +/- 7.24 was reduced to 24.4 +/- 6.12 ng/ml by the end of the 6-month therapy (p less than 0.001). Serum alkaline phosphatase also was reduced by 64.4%. Three out of 19 patients suffered from hypercalcemia during the 4th month of therapy. Calcium supplement given to 6 other patients with severe secondary hyperparathyroidism did not lower serum PTH levels significantly after 6 weeks of therapy, although serum calcium levels increased and were sustained above 10 mg/dl for the last 5 weeks. These findings strongly suggest that the suppressive effect of the oral 1,25(OH)2D3 pulse therapy was attained by a direct action of 1,25(OH)2D3 on the parathyroid gland rather than by its ability to elevate serum calcium levels. In conclusion, the oral 1,25(OH)2D3 pulse therapy effectively lowered PTH levels in hemodialysis patients who cannot tolerate large daily doses of 1,25(OH)2D3.

Administration, Oral↗
PubMed1991

Time course of released atrial natriuretic peptide after acute myocardial infarction.

The plasma concentration of atrial natriuretic peptide (pANP) was investigated at fixed times during 48 h following the onset of an initial attack of mild acute myocardial infarction (AMI) in 11 patients. Six hours after onset, the mean pANP was elevated, but 6 h later pANP had returned to the baseline level. Forty-eight hours after onset the mean pANP increased again. Thus, the curve of the time course of pANP consisted of 2 peaks separated by a dip. Six hours after onset, systemic hemodynamics and humoral factors were measured in 27 patients. At 48 h they were measured in 14 patients. The late elevation of pANP correlated with mean pulmonary arterial wedge pressure (r = 0.63, n = 14, p less than 0.05), while the early elevation of pANP did not (r = 0.31, n = 27, n.s.). The early elevation of pANP correlated with plasma concentrations of both noradrenaline (r = 0.55, n = 27, p less than 0.01) and creatine phosphokinase (r = 0.54, n = 27, p less than 0.01). In addition, noradrenaline levels positively correlated with mean pulmonary arterial wedge pressure (r = 0.38, n = 27, p less than 0.05). The cause of the early elevation of pANP in AMI is unclear, but it is suggested that injury to myocardium and activated sympathetic nerve activity may be responsible in part.

Atrial Natriuretic Factor↗
PubMed1991

[Histopathological study of aortic wall dissection].

To determine the etiology of aortic wall dissection, a histopathological study of the aorta in 20 cases with dissecting aortic aneurysm (DA), 3 cases with Marfan syndrome and 3 cases with annulo-aortic ectasia (AAE) was performed. Controls consisted of 348 cases of normally-aging aorta. In cases with aortic wall dissection, the histopathological changes in the undissected media were also carefully examined. In Marfan syndrome and AAE, there was a marked accumulation of acid mucopolysaccharide (AMPS) and its distribution in the wall was diffuse in patients under 50 years old, resulting in changes in elastic fibers including fragmentation, elastolysis and reticulation. In contrast, DA was histopathologically characterized by zonal fibrosis and abnormally-dilated vessels in the aortic media. These lesions were found in 8 (40%) of the 20 DA cases. The remaining 12 cases also had increased vascularization and fragmentation of elastic fibers. This medial fibrosis and increased vascularization were particularly marked in older patients. Among the 3 diseased entities responsible for aortic wall dissection, DA differed distinctly from Marfan syndrome or AAE as to the amount and site of AMPS accumulation in the media as well as fibrosis and hypervascularity in the outer half of the aortic media. In conclusion, aortic wall dissection in younger patients may be etiologically associated with the increased AMPS accumulation in the aortic media which may always be accompanied by degeneration of elastic fibers in this study, however, in older patients zonal fibrosis and abnormal vessels developing in the media are responsible for the dissection.

Adolescent↗
PubMed1990

Noninvasive evaluation of the magnitude of aortic and mitral regurgitation by means of Doppler two-dimensional echocardiography.

Using transmitral flow velocity and left ventricular ejection flow velocity, we measured left ventricular inflow volume (LVIV) and left ventricular outflow volume (LVOV) by pulsed Doppler echocardiography in 73 patients who had mitral valve regurgitation (MR), aortic valve regurgitation (AR), or no valvular regurgitation. Doppler-determined regurgitant volume (DOPRV), Doppler-determined regurgitant fraction (DOPRF), total stoke volume, and forward stroke volume were calculated to compare the severity assessed by angiographic scoring and the regurgitant fraction determined by radionuclide angiography (RIRF). In 17 patients with MR, LVIV (84.4 +/- 20.4 ml) was significantly greater (p less than 0.01) than LVOV (52.5 +/- 15.7 ml). LVOV, which is equivalent to forward stroke volume, was lower in patients with MR (52.2 +/- 15.7 ml) than in normal subjects (67.0 +/- 15.7 ml). In 15 patients with AR, LVOV (121.7 +/- 61.1 ml) was significantly greater (p less than 0.01) than LVIV (75.1 +/- 28.1 ml) and LVOV, which is equivalent to total stroke volume, was greater in patients with AR (121.7 +/- 61.1 ml) than in normal subjects (64.0 +/- 14.4 ml). DOPRF correlated with RIRF (r = 0.79, p less than 0.01, n = 11). DOPRV (mild: 10.5 +/- 8.5 ml; moderate: 28.8 +/- 13.6 ml; severe: 74.5 +/- 36.7 ml) and DOPRF (mild: 13.7% +/- 11.5%; moderate: 33.1% +/- 14.2%; severe: 52.6% +/- 15.3%) increased markedly with the severity of regurgitation as assessed by cineangiography. In AR, total stroke volume influenced both forward stroke volume and regurgitant volume, and in MR, regurgitant volume influenced both total stroke volume and forward stroke volume. Total stroke volume in AR and regurgitant volume in MR may play a key role in valvular regurgitation.

Adolescent↗
PubMed1990

The role of the left ventricle in atrial natriuretic peptide secretion in acute mitral regurgitation.

To examine the role of the ventricle in ANP secretion, the atrial natriuretic peptide (ANP) concentration in the plasma, left atrial tissue and left ventricular tissue were observed in a canine during the course of experimental reversible mitral regurgitation (MR). For reversible MR, a basket catheter was inserted into the left atrium via the pulmonary vein and fixed at the mitral valve. The regurgitation arose when the tip basket wire was extended and disappeared immediately when it was closed. Left atrial pressure (LAP), right atrial pressure (RAP) and pulmonary artery pressure (PAP) increased significantly during MR, and decreased to the normal level after recovery from MR. Plasma ANP concentration showed a reversible change in correlation with LAP and RAP in each canine studied. The ANP level in the atrial and ventricular tissue decreased during MR, and the low levels were maintained after recovery from MR. Both the left arterial and left ventricular tissue ANP levels showed the same changes in acute MR. Therefore, it was suggested that normal ventricles might play a role in ANP secretion in acute MR.

Animals↗
PubMed1990

Hemodynamic changes by recombinant erythropoietin therapy in hemodialyzed patients.

Recombinant human erythropoietin therapy was given to 15 patients undergoing long-term hemodialysis with normal cardiac function. None of the patients had hypertension before the erythropoietin therapy and had received no antihypertensive agents. Before and after the erythropoietin therapy M-mode and pulsed Doppler echocardiographic studies, measurements of plasma volume by radioiodinated human serum albumin, and measurements of atrial natriuretic factor were carried out. After 6 weeks of erythropoietin therapy, hematocrit increased from 20.0 to 33.0%. Cardiac output, stroke volume, left ventricular diastolic dimensions, and left ventricular wall stress were all significantly decreased. Total peripheral resistance, interventricular septal thickness, and left ventricular posterior wall thickness were significantly increased. In Doppler echocardiographic studies, the mean velocity of aortic ejection flow and left ventricular acceleration time were decreased. The blood volume derived from plasma volume and hematocrit was not changed, whereas plasma atrial natriuretic factor concentration was significantly decreased. These data suggest that recombinant human erythropoietin administration suppressed the hyperdynamic cardiac state that was required to maintain oxygen delivery to the peripheral tissues in severe uremic anemia.

Adult↗
PubMed1990

[Studies of hyperkinetic circulatory state in chronic anemia].

To clarify the hemodynamics of anemia, 28 patients with iron deficiency anemia were investigated in respect to their parameters of left ventricular (LV) systolic and diastolic function. The subjects were categorized in three groups: 1) patients (pts) with severe anemia, whose hemoglobin (Hb) concentration was less than 7 g/dl (N = 7); 2) pts with moderate anemia, whose Hb concentration was between 7 and 10 g/dl (N = 13): and 3) pts with mild anemia whose Hb concentration was between 10 and 12 g/dl (N = 8). Changes in hemodynamic parameters were observed before and after treatment in 14 subjects. These results were compared with those of normal subjects (N = 11). In the anemic patients, LV stroke volume (SV), and heart rate both increased. An increase in SV was accompanied by an increase in LV preload (LV diastolic diameter = LVDd by M-mode echocardiography) and an increase in the Doppler parameters of early diastolic filling (peak velocity in the rapid filling phase, acceleration rate, and deceleration rate). SV correlated roughly with LVDd (r = 0.44, p less than 0.05). In addition, the indices of LV contractility as measured by the pulsed Doppler method (ET/PEP) and by M-mode echocardiography (mVcf) also increased. These factors which contributed to hyperkinetic circulation were restored as the anemia improved. It was concluded that an increase in SV is an important determinant of high cardiac output in chronic anemia, because it parallels the severity of anemia. The change in SV is preload-dependent, and is suspected of being LV contractility-dependent.

Adolescent↗
PubMed1990

[Left ventricular asynergy and myocardial necrosis accompanied by subarachnoid hemorrhage: contribution of neurogenic pulmonary edema].

One hundred-thirty patients with acute subarachnoid hemorrhages were investigated to examine the relationship of neurogenic pulmonary edema to cardiac lesions. Abnormal electrocardiograms were observed in 99 of these patients. Left ventricular asynergy was detected in nine of the 99 patients by two-dimensional (2D) echocardiography. In addition to 2D echocardiography, chest radiography, electrocardiography, serum CPK measurements and cardiac catheterization were performed for these nine patients in the acute stages of their subarachnoid hemorrhages. Abnormal electrocardiographic findings included prolongation of QT intervals and marked ST-T changes, which were observed in all nine patients. Pulmonary edema associated with increased pulmonary arterial wedge pressures were noted in seven, and increases in CPK and MB-CPK in all patients, suggesting the occurrence of myocardial necrosis. An increase in serum catecholamine was observed in all patients. Coronary angiography was performed in two patients and revealed normal coronary arteries in both. Biopsy findings were available in three and demonstrated severe fragmentation at the sites of left ventricular asynergy. Pulmonary edema, electrocardiographic abnormalities and left ventricular asynergy improved markedly during the courses of hospitalization. We concluded that left ventricular asynergy and myocardial necrosis may occur during the acute stage of subarachnoid hemorrhage and could produce neurogenic pulmonary edema rather than or in addition to permeability edema.

Adult↗
PubMed1990

[A case report of corrected transposition of the great arteries without any associated defects in a 36-year-old man and the review of adult cases reported in Japan].

We report a case in a 36-year-old man of corrected transposion of the great arteries (CTGA) without any associated defects. We also review clinical characteristics and later complications of adult CTGA cases reported in Japan. The patients was referred to our hospital for further examination of the abnormal ECG found during regular medical check-up. His ECG showed left axis deviation, first degree AV block, abnormal Q waves in the left precordial leads, and disappearance of septal q waves in the left precordial leads. His exercise capacity was found to be more than 12 METS by treadmill exercise testing. His roentgenogram revealed an egg-shaped ventricle with normal CTR (45%). The following findings were obtained by two-dimensional echocardiogram and heart catheterization: 1) the functional left ventricle had the characteristics of the anatomical right ventricle, 2) The positions of the left and right atrioventricular valves were reversed, 3) Other cardiac anomalies such as VSD, pulmonary stenosis, tricuspid regurgitation (TR) were not proved. Therefore, he was diagnosed as having CTGA without any cardiac defects (SLL type). At present, with ages more than 15 years, 36 cases of CTGA without cardiac anomalies have been reported in Japan including this case. But most cases had significant TR. This case was the 7th reported case without the accompaniment of TR. Among 36 cases, TR was found in 71%, complete AV block in 20%, and congestive heart failure was noted in 45%. Prognosis of CTGA without any defects is dependent on the appearance of TR, advanced AV block, and congestive heart failure. As these later fatal complications are observed very often, it is important to detect the patient of CTGA accurately.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[The concentration of atrial natriuretic peptide (ANP) in plasma and atrial tissue of canines with acute heart failure induced by reversible aortic or mitral regurgitation].

We have established an easily reversible acute heart failure model in beagle canines by reversible aortic or mitral regurgitation (AR or MR). To cause reversible AR, a basket catheter was inserted into the left ventricle from the apex and fixed at the aortic valve in 10 canines. To cause MR, a basket catheter was inserted into the left atrium via the pulmonary vein and fixed at the mitral valve in 10 canines. The regurgitation by AR or MR was caused by extending the tip basket wire, and the recovery from the regurgitation was immediately possible by closing it. Left atrial pressure (LAP), right atrial pressure (RAP) and pulmonary artery pressure (PAP) were increased significantly during AR or MR, and decreased to the normal level after the release of AR or MR. Using these reversible acute heart failure models, the effects of both advancing and restoring acute heart failure by the secretion of ANP were examined by observing the changes of ANP concentration and its molecular forms in the plasma and left atrial tissue in the same canine. Plasma ANP concentration showed a reversible change. In group analysis, plasma ANP concentration did not correlate with LAP or RAP, but in each canine it showed high correlations with LAP (r = 0.70 approximately 0.94, 0.82 +/- 0.07) and RAP (r = 0.60 approximately 0.93, 0.79 +/- 0.08), having a different slope in each regression line. The ANP concentration in the atrial tissue was decreased during AR or MR, but the low level was maintained after AR or MR. The main molecular form of ANP in the plasma was alpha-ANP and that in the tissue was gamma-ANP. In summary, the tissue storage of ANP was decreased because the ANP secretion caused by stimulation of acute heart failure exceeded its production. The ANP secretion was decreased by the subsequent elimination of heart failure, but the production was not stimulated rapidly, because the tissue content remained unchanged.

Acute Disease↗
PubMed1989

No specific organ removes atrial natriuretic peptide from the human plasma.

The fate of atrial natriuretic peptide (ANP) was studied by arterial and venous catheterization in ischemic heart disease patients, and arterio-venous blood sampling in healthy kidney donors at the time of transplantation. In vitro ANP degradation was examined using healthy human plasma. In ischemic heart disease, the plasma ANP concentration at the inferior vena cava was 62.6% of that at the left ventricle, and that at the superior vena cava was 82.8%. Arterio-venous gradients were similar from pulmonary artery to vein (88.3%), from celiac artery to the hepatic vein (75.5%) and from the femoral artery to vein (85.4%). In the donor for kidney transplantation, renal arterio-venous gradient was also similar at 77.1%. No platelet consumption of ANP was noted, and the molecular forms of ANP present in the circulation were similar in samples obtained from both the coronary sinus and the superior or inferior vena cava. We conclude that no specific organ plays a dominant role in ANP degradation, and that ANP molecular forms may not be altered during circulation.

Adolescent↗
PubMed1989

[Echocardiographic study of a cardiac murmur in cor triatriatum: a case report].

This is a report of an aged patient with cor triatriatum in whom the mechanism of his cardiac murmur was elucidated by Doppler and contrast echocardiography. This 63-year-old man was followed up for cardiomegaly detected at 40 years of age, and he had been treated for a cardiac murmur due to valvular disease during the previous 10 years. He was admitted to our hospital for the evaluation of incidental hematemesis. A phonocardiogram recorded over the apex showed a regurgitant murmur from early to mid-systole, followed by a continuous murmur lasting up to mid-diastole. Two-dimensional echocardiogram revealed an abnormal septum in the left atrium dividing the atrium into two chambers and showing bulging in late systole through diastole. In the lower chamber, color Doppler echocardiography disclosed continuous turbulent flow originating from the bulge directing the mitral orifice. Contrast medum coursing toward the mitral orifice was demonstrated during contrast echocardiography and left ventriculography, which coincided with the turbulent signal on the Doppler echocardiogram. The description of the cardiac murmur of cor triatriatum suggests that it is not persistent. Conceivably, it is a continuous murmur, whose mechanism can be elucidated by Doppler and contrast echocardiography.

Contrast Media↗
PubMed1989

[Effect of recombinant human erythropoietin administration on cardiovascular system in patient with chronic renal failure: an analysis of the blood pressure upward].

To investigate the mechanism of blood pressure upward after recombinant human erythropoietin (EPO) administration in patient with chronic renal failure (CRF), hemodynamic changes following on the improvement of anemia was evaluated by the echocardiography. Fourteen (5 males, 9 females) normotensive patients with less than 23% of hematocrit (HT) were administered 1,500 approximately 3,000 units of EPO three times a week. Four patients with systolic (greater than 160 mmHg) or diastolic (greater than 90 mmHg) hypertension after EPO administration was named group H, the remaining patients was named group N. Blood pressure, heart rates and parameters of echocardiography examined after the improvement of anemia were compared to those examined before EPO administration, respectively. Patients had an increase in Ht from 20.0 +/- 1.6% to 33.0 +/- 1.9% (p less than 0.01). LVDd, LVEDV, CO and flow velocity in group N were significantly decreased after EPO administration; while those in group H did not show the significant changes. IVSth and LVPWth in each group were significantly increased after EPO administration. These data showes that decrease in CO maintains the patients normotensive after EPO administration.

Adult↗
PubMed1988

Noninvasive evaluation of the ratio of pulmonary to systemic flow in ventricular septal defect by means of Doppler two-dimensional echocardiography.

Left ventricular inflow volume (LVIV) and outflow volume (LVOV) were determined by pulsed Doppler echocardiography, and the ratio of pulmonary to systemic flow (Qp/Qs) was estimated as a ratio of LVIV to LVOV (LVIV/LVOV). Seventy-seven patients were studied, 47 control subjects and 30 patients with ventricular septal defect (VSD). LVOV was calculated from the left ventricular ejection flow velocity and left ventricular outflow tract diameter; LVIV was calculated from the transmitral flow velocity and mitral valve motion as traced by M-mode echocardiography. Cardiac input (COin) and cardiac output (COout) were calculated as the product of LVIV or LVOV and heart rate. Cardiac output was also determined by the dye dilution method (COdye) in control subjects. A close correlation was observed between COdye and COin (y = 1.18x - 243, r = 0.85, p less than 0.005, SEE = 1026 ml/min) and COdye and COout (y = 1.16x - 323, r = 0.90, p less than 0.005, SEE = 639 ml/min). LVIV and LVOV were highly correlated in control subjects (y = 0.95x + 5.3, r = 0.94, p less than 0.005, SEE = 6.6 ml). LVIV/LVOV was 0.97 +/- 0.1 (mean +/- SD) in control subjects, whereas LVIV/LVOV (1.87 +/- 0.88) was significantly higher in patients with VSD (p less than 0.01). In patients with VSD, LVIV/LVOV correlated with Qp/Qs determined invasively (y = 0.97, SEE = 0.23, n = 16). Thus with our method LVIV and COin can be accurately determined, and we suggest that Doppler-determined LVIV/LVOV is clinically useful for evaluating the shunt flow magnitude in VSD.

Adult↗